Cerebral vasodilation during hypercapnia: Role of glibenclamide-sensitive potassium channels and nitric oxide

Abstract

Background and Purpose The purpose of these experiments was to examine mechanisms by which hypercapnia produces vasodilatation in brain. We examined the hypothesis that dilatation of cerebral arterioles during hypercapnia is dependent on activation of ATP-sensitive potassium channels and formation of nitric oxide. Methods Diameters of cerebral arterioles were measured using a closed cranial window in anesthetized rabbits. Changes in diameter of arterioles were measured in response to topical application of acetylcholine and sodium nitroprusside and during two levels of systemic hypercapnia. Results Increasing arterial PCO2 from 32 ± 1 mm Hg (mean±SE) to 54 ± 1 and 66 ± 1 mm Hg dilated cerebral arterioles by 25 ± 3% and 38 ± 5%, respectively, from a control diameter of 93 ± 3 turn. The response to the low level of hypercapnia was attenuated (25 ± 3% versus 16 ± 4%, P